Exploring the neurological substrate of emotional and social intelligence

被引:300
作者
Bar-On, R
Tranel, D
Denburg, NL
Bechara, A
机构
[1] Univ Iowa, Coll Med, Dept Neurol, Div Behav Neurol & Cognit Neurosci, Iowa City, IA 52242 USA
[2] Trent Univ, Emot Intelligence Res Lab, Peterborough, ON K9J 7B8, Canada
关键词
social cognition; decision-making; emotion; somatic markers; emotional intelligence;
D O I
10.1093/brain/awg177
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The somatic marker hypothesis posits that deficits in emotional signalling (somatic states) lead to poor judgment in decision-making, especially in the personal and social realms. Similar to this hypothesis is the concept of emotional intelligence, which has been defined as an array of emotional and social abilities, competencies and skills that enable individuals to cope with daily demands and be more effective in their personal and social life. Patients with lesions to the ventromedial (VM) prefrontal cortex have defective somatic markers and tend to exercise poor judgment in decision-making, which is especially manifested in the disadvantageous choices they typically make in their personal lives and in the ways in which they relate with others. Furthermore, lesions to the amygdala or insular cortices, especially on the right side, also compromise somatic state activation and decision-making. This suggests that the VM, amygdala and insular regions are part of a neural system involved in somatic state activation and decision-making. We hypothesized that the severe impairment of these patients in real-life decision-making and an inability to cope effectively with environmental and social demands would be reflected in an abnormal level of emotional and social intelligence. Twelve patients with focal, stable bilateral lesions of the VM cortex or with right unilateral lesions of the amygdala or the right insular cortices, were tested on the Emotional Quotient Inventory (EQ-i), a standardized psychometric measure of various aspects of emotional and social intelligence. We also examined these patients with various other procedures designed to measure decision-making (the Gambling Task), social functioning, as well as personality changes and psychopathology; standardized neuropsychological tests were applied to assess their cognitive intelligence, executive functioning, perception and memory as well. Their results were compared with those of 11 patients with focal, stable lesions in structures outside the neural circuitry thought to mediate somatic state activation and decision-making. Only patients with lesions in the somatic marker circuitry revealed significantly low emotional intelligence and poor judgment in decision-making as well as disturbances in social functioning, in spite of normal levels of cognitive intelligence (IQ) and the absence of psychopathology based on DSM-IV criteria. The findings provide preliminary evidence suggesting that emotional and social intelligence is different from cognitive intelligence. We suggest, moreover, that the neural systems supporting somatic state activation and personal judgment in decision-making may overlap with critical components of a neural circuitry subserving emotional and social intelligence, independent of the neural system supporting cognitive intelligence.
引用
收藏
页码:1790 / 1800
页数:11
相关论文
共 45 条
  • [1] [Anonymous], 1983, DEV CHILDRENS THOUGH
  • [2] [Anonymous], 1956, Nonparametric statistics for the behavioral sciences
  • [3] [Anonymous], 2000, HDB EMOTIONAL INTELL
  • [4] Bar-On R., 2000, Handbook of Emotional Intelligence
  • [5] Bar-On R., 1997, BARON EMOTIONAL QUOT
  • [6] Bar-On R., 2001, EMOTIONAL INTELLIGEN, P82
  • [7] BARON R, 2003, IN PRESS EMOTIONAL I
  • [8] Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal region
    Barrash, J
    Tranel, D
    Anderson, SW
    [J]. DEVELOPMENTAL NEUROPSYCHOLOGY, 2000, 18 (03) : 355 - 381
  • [9] Characterization of the decision-making deficit of patients with ventromedial prefrontal cortex lesions
    Bechara, A
    Tranel, D
    Damasio, H
    [J]. BRAIN, 2000, 123 : 2189 - 2202
  • [10] Bechara A, 1998, J NEUROSCI, V18, P428